Immunosuppressive properties of the Mycoplasma arthritidis T-cell mitogen in vivo: inhibition of proliferative responses to T-cell mitogens.

AUTOR(ES)

Cole, B C

RESUMO

We have previously shown that Mycoplasma arthritidis produces a soluble T-cell mitogen (MAM) which is active for most mouse strains that express the alpha chain of the I-E molecule (E alpha) encoded within the murine major histocompatibility complex. The lymphocytes from mice injected intravenously with the MAM exhibited a marked decrease in their ability to respond in vitro to MAM, to phytohemagglutinin, or to concanavalin A T-cell mitogens. Suppression could only be induced in MAM-responsive mouse strains and was most marked 1 to 4 days postinjection. Splenic and node cells and, to a lesser extent, thymic cells from MAM-injected mice could inhibit the ability of lymphocytes from normal mice to respond to MAM and lectin mitogens. A minimum of 2.5 x 10(4) viable cells was required for significant transfer of suppression, and no major histocompatibility complex restrictions were seen. Unlike concanavalin A-induced suppressor cells, which consist of a CD4-, CD8+ T-cell subset, suppressor cells induced by MAM were due to a CD4+ CD8- subset. We hypothesize that MAM may play a role in M. arthritidis-mediated disease by both its inflammatory and immunosuppressive properties.

Documentos Relacionados

• Human T-cell responses to Mycoplasma arthritidis-derived superantigen.
• T4+ T helper cell function in vivo: differential requirement for induction of antiviral cytotoxic T-cell and antibody responses.
• Crosstalk between alpha/beta T cells and gamma/delta T cells in vivo: activation of alpha/beta T-cell responses after gamma/delta T-cell modulation with the monoclonal antibody GL3.
• Relative contribution of "determinant selection" and "holes in the T-cell repertoire" to T-cell responses.
• Inhibitors of glycoprotein processing alter T-cell proliferative responses to antigen and to interleukin 2.